Telomeres shorten with age in many human tissues and such shortening may play a role in the aging process. Werner syndrome (WS) is a recessive genetic disorder characterized by the premature onset of several features of aging. Cells from Werner patients senesce and shorten telomeres at a much faster rate compared to normal cells. Accumulating evidence indicates that the protein deficient in WS, WRN, functions in telomere maintenance. Since cells must preserve proper telomere function for continued survival, and may use homologous recombination to repair shortened telomeres, this proposal attempts to determine whether WRN and its homologues participate in telomere recombination as a way to repair or protect shortened telomeres. Understanding how the Werner syndrome family proteins are involved in telomere maintenance should yield insight into the natural processes of aging.